As prior studies verified increased expression of xCT and GCLC in TSC 4, 11, dysmorphic cells in TSC and FCD IIb likely increase Nrf‐2 activity to adapt to increased intracellular iron caused by mTOR activity, while paradoxically producing even more labile iron via HO‐1. The gene discussed is SLC7A11; the disease is fleck corneal dystrophy.